2. Academic Validation
  3. Inhibition of BRD4 expression attenuates the inflammatory response and apoptosis by downregulating the HMGB-1/NF-κB signaling pathway following traumatic brain injury in rats

Inhibition of BRD4 expression attenuates the inflammatory response and apoptosis by downregulating the HMGB-1/NF-κB signaling pathway following traumatic brain injury in rats

  • Neurosci Lett. 2023 Jul 7;137385. doi: 10.1016/j.neulet.2023.137385.
Yongkui Zhu 1,  Haibo Ni 2,  Qian Chen 1,  Huan Qian 3,  Yiling Fang 4,  Rong Gao 5,  Bofei Liu 6
Affiliations

Affiliations

  • 1 Department of Intensive Care Unit, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
  • 2 Department of Neurosurgery, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China; Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China.
  • 3 Department of Anesthesia, Zhangjiagang Hospital of Traditional Medicine, Suzhou, China.
  • 4 Department of General Practice, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
  • 5 Department of Neurosurgery, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China. Electronic address: gaorong_zjg@163.com.
  • 6 Department of Intensive Care Unit, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China. Electronic address: liubofei.zjg.js@163.com.
PMID: 37423465 DOI: 10.1016/j.neulet.2023.137385
Abstract

Neuroinflammation plays an important part in secondary traumatic brain injury (TBI). Bromodomain-4 (BRD4) exerts specific proinflammatory effects in various neuropathological conditions. However, the underlying mechanism of action of BRD4 after TBI is not known. We measured BRD4 expression after TBI and investigated its possible mechanism of action. We established a model of craniocerebral injury in rats. After different intervention measures, we used western blotting, immunofluorescence, real-time reverse transcription-quantitative polymerase chain reaction, neuronal Apoptosis, and behavioral tests to evaluate the effect of BRD4 on brain injury. At 72 h after brain injury, BRD4 overexpression aggravated the neuroinflammatory response, neuronal Apoptosis, neurological dysfunction, and blood-brain-barrier damage, whereas upregulating expression of HMGB-1 and NF-κB had the opposite effect. Glycyrrhizic acid could reverse the proinflammatory effect of BRD4 overexpression upon TBI. Our results suggest that: (i) BRD4 may have a proinflammatory role in secondary brain injury through the HMGB-1/NF-κB signaling pathway; (ii) inhibition of BRD4 expression may play a part in secondary brain injury. BRD4 could be targeted therapy strategy for brain injury.

Keywords

Apoptosis; BRD4; Inflammation; Traumatic brain injury.

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